Abstract
The treatment of peripheral arterial occlusive disease has two aspects - one is aimed at improving the prognosis (intervention risk factors for atherothrombosis), the second on improving the quality of life, especially the improvement of tolerance walk. In this second strategy, cilostazol has an important position.
The mechanism of action is twofold: inhibition of phosphodiesterase isoenzyme 3A retards the biodegradation of cyclic nucleotides (cAMP and cGMP). Increasing the supply of these "second messengers" results in smooth muscles of vascular wall vasodilation, and to stabilisation and reduced response to activating stimuli of platelets.
Parallel cilostazol inhibits transporter ENT-1 facilitating transmembraneous transport of adenosine. This increases its offer and stimulates purinergic receptors in tissues.
This activity leads to an increase in supply of cAMP in the vessel wall and the platelet, and potentiates the effect of inhibition of phosphodiesterase. Indication of cilostazol is symptomatic treatment of patients in the stage of claudication.
The significant prolongation of painless and maximum claudication interval has been proven. Tolerance of cilostazol is good.
Only adverse effects that are own to all vasodilatant agents occurred more frequently, i.e. headaches, palpitations and perimalleolar swelling. Treatment safety was excellent, there was no increased incidence of bleeding observed.
The evaluation in the last recommended procedures TASC II is in accordance with these characteristics, wherein it is stated that cilostazol is the drug with the highest proven benefit for patients with claudication.